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Pectolinarigenin attenuates hepatic ischemia/reperfusion injury via activation of the PI3K/AKT/Nrf2 signaling pathway.
- Source :
-
Chemico-Biological Interactions . Dec2023, Vol. 386, pN.PAG-N.PAG. 1p. - Publication Year :
- 2023
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Abstract
- Hepatic ischemia/reperfusion (I/R) injury is an unavoidable complication of liver hepatectomy, transplantation, and systemic shock. Pectolinarigenin (Pec) is a flavonoid with many biological activities, which include anti-inflammatory, anti-apoptotic, and antioxidant stress. This study explored whether Pec pretreatment could reduce hepatic I/R injury and the potential mechanisms at play. After pretreatment of mice and AML12 cells with Pec, I/R and hypoxia/reoxygenation (H/R) models were established. By examining markers related to liver injury, cell viability, oxidative stress, inflammatory response, and apoptosis, the effect of Pec on important processes involved in hepatic I/R injury was assessed. Protein levels associated with the PI3K/AKT/Nrf2 pathway were analyzed by relative quantification to investigate possible pathways through which Pec plays a role in the I/R process. Pec treatment corrected abnormal transaminase levels resulting from I/R injury, improved liver injury, and increased AML12 cell viability. Moreover, Pec treatment inhibited oxidative stress, inflammation and apoptosis and could activate the PI3K/AKT/Nrf2 pathway during I/R and H/R. Further studies found that LY294002 (PI3K inhibitor) suppressed the protective effect of Pec on hepatic I/R injury. In summary, our results show that Pec inhibits oxidative stress, inflammatory responses, and apoptosis, thereby attenuating I/R-induced liver injury and H/R-induced cell damage via activation of the PI3K/AKT/Nrf2 pathway. • Pectolinarigenin pretreatment can attenuate hepatic ischemia/reperfusion injury. • Pectolinarigenin reduces hypoxia/reoxygenation-induced AML12 cell damage. • Pectolinarigenin inhibits oxidative stress, inflammation and apoptosis during ischemia/reperfusion. • Pectolinarigenin exerts protective effects through activation of the PI3K/AKT/Nrf2 pathway. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00092797
- Volume :
- 386
- Database :
- Academic Search Index
- Journal :
- Chemico-Biological Interactions
- Publication Type :
- Academic Journal
- Accession number :
- 173629599
- Full Text :
- https://doi.org/10.1016/j.cbi.2023.110763